As is well known, a knee joint consists of an inside and an outside. It has often been believed that the knee pain is caused by problems of the inside of the joint. However, receptors, which function to transport pain, are more present around the joint than the inside of the joint. Furthermore, autoradiography reveals that the level of knee injury is not necessarily directly proportional to the level of pain in the knee. With age, a man typically has injury to the inside of the joint while the outside of the joint undergoes various changes.
The saphenous nerve is a nerve that transfers the pain of the medial side of the knee. The entrapment of the nerve also causes pain in the knee. Although the saphenous nerve entrapment can be identified by electroneuromyography, etc., the saphenous nerve is oftentimes not entrapped when the nerve is in a rest state. As such, it is virtually impossible to diagnose the entrapment by electroneuromyography when the nerve is in the rest state. (See, Schon L C, Baxter D E. Neuropathies of the foot and ankle in athletes, Clin Sports Med. 1990 April; 9(2): 489-509, Mens J M. Pseudoarthritis of the knee caused by compression neuropathy of the saphenous nerve, Ned Tijdschr Geneeskd, 1987 Jul. 11; 13 1(28): 1215-8, Morganti C M, McFarland E G, Cosgarea A J. Saphenous neuritis: a poorly understood cause of medial knee pain, J Am Acad Orthop Surg. 2002 March-April; 10(2): 130-7). The saphenous nerve entrapment is a condition that occurs frequently. However, a drug which efficiently treats the pain associated therewith has not been developed.
The anaerobic, gram positive bacterium Clostridium botulinum produces a botulinum toxin. Such toxin causes a neuroparalytic illness in humans and animals known as botulism. The effects of botulism typically appear about 18 to 36 hours after eating foods infected with Clostridium botulinum spores. The botulinum toxin can apparently pass through the lining of the gut and attack the peripheral motor neurons.
Botulinum toxins have been used in clinical settings for the treatment of neuromuscular disorders characterized by hyperactive skeletal muscles. Botulinum toxin type A has been approved by the U.S. Food and Drug Administration for the treatment of blepharospasm, strabismus and hemifacial spasm. Non-type A botulinum toxin serotypes apparently have lower potency and/or shorter duration of activity than botulinum toxin type A. Clinical effects of peripheral intramuscular botulinum toxin type A are usually seen within one week of injection. A typical duration of symptomatic relief from a single intramuscular injection of botulinum toxin type A averages about three months.
Although techniques for treating pain through the use of botulinum toxin have been developed, the botulinum toxin used in the prior art focused on the effect of the toxin on the acetylcholine per se.
For example, U.S. patent publication 2003/0224019 is directed to the use of botulinum toxin type B for treating pain caused by nerve entrapment. It specifies that the botulinum toxin type B is injected into an area where nerve entrapment occurs. This may also include an area impinging the nerve itself or near the nerve. In the publication, the duration of effect in patients responding to MYOBLOC™ treatment has been observed to be between 12 and 16 weeks at a dosage of 5,000 units or 10,000 units.
The use of botulinum toxin type A has been disclosed in U.S. patent publication 2004/028704. In that publication, the botulinum toxin type A is utilized for treating pain caused from carpal tunnel syndrome. Further in that publication, the botulinum toxin type A is injected into muscles of the hand andor wrist, or the carpal tunnel along the median nerve.
U.S. patent publication 2004/038874 discloses that the botulinum toxin treats pain by blocking acetylcholine andor neurotransmitter rather than directly affecting the receptors. However, it does not specify the area to be injected.
Furthermore, WO 2001/78760 describes a method for treating pain through peripheral administration of botulinum toxin to a patient who is experiencing a nonmuscle disorder related pain. However, the botulinum toxin in that method is not injected into a certain treatment area identified by a physical scientific examination. It is rather randomly injected into a non-specified area, thereby exhausting acetylcholine and controlling pain by a chemically mediated response. Thus, such method is not intended to treat a specific disease.
Although, the prior art references describe that the pain could be treated by using the botulinum toxin, they fail to teach or suggest treating the pain in the knee joint rapidly and effectively through injecting a lower amount of botulinum toxin. Currently, there is a need for a drug which can be applied effectively to treat the pain in the knee joint.